Nutrition Science For Dentistry

Tobias K. Boehm

Why do we care?

Out in the ocean, seafarers have long known a dreadful disease that befalls those who don’t eat well.

Hear Antonio Pigafetta, who travelled with Magellan on his voyage across the globe in the 15th century,

describe the particular horror that befell his fellow men while out in the middle of the Pacific Ocean:

“We had been three months and twenty days without taking refreshment of any kind. We ate

biscuit which was no longer biscuit, but powder with handfuls of maggots because these

creatures had eaten the good part. It smelled strongly of rat urine. We drank water that was

yellow and putrefied for many days, and we ate certain cowhides which were placed over the

main yard so that the yard should not break the shrouds, hardened by sun, rain and wind. We

left the hides in the seas for four or five days…Many times we ate sawdust. Rats were sold for

half a ducat each, when we could get them.

But above all other calamities this was the worst: in some men the gums grew over the teeth,

both lowers and uppers, so that they could not eat in any way and thus they died of this

sickness. Nineteen men died and also the Patagonian giant and an Indian from the land of Brazil.

Twenty-five or thirty men became sick, some in the arms, in the legs or other places, so that few

remained healthy.

By the grace of God I had no sickness.”

(Translated excerpt from “Il Primo Viaggio Intorno Al Mondo di Antonio Pigafetta” , edited by C.

Manfroni 1928)

This is one of the early accounts of how poor nutrition resulted in deadly oral disease, and subsequent

generations of seafarers in the age of sail feared this condition more than most other disasters, as it was

bound to happen on any long distance voyage. It took well into the 19th century to understand the role

of food in preventing malnutrition states like scurvy, and to develop techniques to that preserved

perishable foods at sea.

Today, it is rare to see such severe forms of malnutrition in developed countries, but you may find a

surprising number of patients who have subtle forms of malnutrition or who may be at risk for becoming

malnourished.

Therefore, let’s review the role of nutrients in the human body, learn to identify patients at risk for

malnutrition and explore different approaches for nutritional counseling.

Scientific underpinnings of Nutritional Science

Since we will be talking about scientific evidence, let’s review some key scientific terms before we get

started. Much of the evidence we present here is based of clinical research.

The simplest and weakest evidence for many nutrition-oral health relationships are based on case

reports where someone describes an unusual disease brought on by poor nutrition. The report on

malnutrition causing oral disease on Magellan’s voyage can also be seen as a case report. If the report

describes several patients who have signs and symptoms associated with malnutrition, we have a little

more evidence in the form of a case series.

Now, since case reports and case series may just document coincidence in rare cases, scientists conduct

a variety of studies to discover consistent associations of oral disease and nutrition. For nutrition, most

studies are cross-sectional in nature, where a large group of subjects is tested for presence of oral

disease. The same group is also assessed for their nutritional status, and correlations between having a

certain nutrient in their diet and oral health are made.

STRENGTH OF EVIDENCE

Expert opinion, CE

Systematic

reviewRandomized

Clinical Trial

Cohort studies

Case-Control studies

Cross-sectional studies

Case reports & series

Animal studies & Benchtop experiments

A

B

C

D

Levels of Evidence (modified from the Oxford Centre for Evidence-based Medicine)

Figure 1: Levels of Evidence (modified from the Oxford Centre for Evidence-based

Medicine)

Since any associations seen in cross-sectional studies may only be coincidence created by another factor

that actually causes oral disease, other study designs are needed. For example, in cohort studies, groups

of subjects that have different nutritional status are followed over a time period to see if one group

develops more oral disease than the other. More proactively, and most likely to imply a cause-effect

relationship are randomized clinical trials, which are very rare for nutrition-oral health relationship

research. In a randomized clinical trial, subjects would be allocated to randomized groups that have

similar characteristics, and one group would receive a certain nutrient while the other group gets

minimal nutrient levels in their diet. Any associations seen here would likely indicate that a nutrient is

indeed responsible for prevention of oral disease.

Clinical research can also consist of reviewing past research, and attempting to mathematically combine

separate research studies into a single study. This is done in a process called meta-analysis, and

essentially indicated if research findings from comparable studies agree with each other. For nutritional

science and oral health, there are not many studies of this kind.

Lastly, there is also basic research, which mostly aims to uncover the underlying mechanisms of clinical

associations. This either involves benchtop research, or animal research, and there are a number of

studies using oral disease models in rats for the study of nutrition effects on oral health.

Here, we will grade available evidence using a scheme similar to that proposed by the Oxford Centre for

Evidence-based Medicine (Figure 1).

The strongest level of evidence, graded as “A”, is given for any findings that have been confirmed by

multiple well-controlled clinical trials and summarized in systematic reviews and meta-analyses.

The next highest level of evidence, graded as “B”, is evidence produced by a well controlled randomized

clinical trial, or if not ethical or feasible to do a clinical trial, evidence from well controlled cohort

studies. These types of experimental designs are the only clinical studies that can demonstrate a likely

cause and effect relationship between a nutritional component and oral health.

We assigned a grade of “C” to cross-sectional studies and well-matched case-control studies as they

produce evidence showing an association between nutrition and oral health. It is more likely with these

retrospective studies that associations could be coincidental, and that findings gained from these

studies may not be predictive for your patients.

Case reports and series were given a “D” grade as they might show interesting cases and drive

hypothesis generation, but most likely are not predictive for your patient’s diagnosis and treatment.

Basic research reports are not given a level of evidence since they may provide mechanisms of nutrition

deficiencies causing disease, but usually are not directly applicable to patient care as rats and cell

cultures may behave differently from complete human beings.

Expert opinion, textbooks and continuing education is also not graded as they often provide correct

information, but usually are not peer-reviewed, and may be skewed by personal values and preferences.

Since quality of the information and usefulness can vary widely, I advise you to critically evaluate these

types of literature individually.

Since many studies on nutrition and oral health are cross-sectional and cohort studies, there are some

statistical terms we need to review.

Often these studies aim to find out if a group of patients with a nutritional characteristic has a lesser or

greater chance of contracting a disease or poor treatment outcome. For each group, the chance of

adverse events can be expressed in terms of risk or odds. Risk is essentially the percentage of patients in

a group that gets a disease or experiences a poor outcome, and is expressed as a number ranging from

zero to one. Likewise, odd ratios are also expressed zero to one, but it represents a ratio of the number

of patients who get a disease over the number of patients who do not get the disease. For instance, if in

a group of one hundred obese patients half of these patients experience worsening of their gum

condition within a year, the risk of worsening gum condition is 0.5, but the odds is 1 since these patients

were as likely to get worsening of their gums than experiencing no further worsening of their gums. As

you can see, the odds are always higher than the risk of an event, but for events happening at very low

frequency, odds and risk values become very similar.

Since the goal of most studies is to find out if a group of patients has a higher change of getting a

disease compared to another group, they usually calculate the risk or odds values for each group and

form ratios of these. A risk ratio is nothing more than the ratio of risk of disease in one group over the

risk of disease in another group, and it is the same with odds ratios. It tends to be easier to understand

risk ratios as they indicate how much more likely a group is getting a disease. If we use the previous

example, and assume that another group of one hundred patients experienced worsening of disease in

twenty-five patients, we know that the risk of disease worsening in non-obese patients is 0.25. As you

remember, the risk of obese patients getting worse disease was 0.5, and you can clearly see that in this

example, obese patients were twice as likely to experience disease worsening as the risk ratio of 0.5

over 0.25 equals 2.

Odds ratios are more difficult to comprehend and they tend to magnify differences. Using the previous

example, the odds of disease worsening in non-obese patients was 25 over 75, or 1/3. As the odds of

disease worsening in obese patients was 1, the odds ratio now is 3 and obese patients have three times

higher odds of getting disease worsening. For most people, this sounds worse than the risk ratio, and

shows how odds ratios magnify differences. Generally, most researchers would find an odds ratio of

equal or less than two not to be an important finding.

In either case, it would be nice to know how likely it is that an observed risk or odds applies to other

groups of patients similar to the one studied. This is where confidence intervals are important. Based on

the number of patients studied, and assuming that research findings will tend to cluster around a certain

value in a normally distributed fashion, it is possible to calculate confidence intervals for risks, odds and

their respective ratios. In essence, a confidence interval typically tells you that you would observe these

numbers 95% of the time if you would repeat the study over and over again, and that most likely you

would observe similar values in your own patients. Provided that results do follow this mathematical

model, and mostly they do, confidence intervals become smaller with increasing subject numbers, and

studies with large samples tend to be more predictive for your patients.

You will hear or see the term “statistically significant” or “significantly different”. This means that there

is a high chance that observed differences are truly different, and usually this is indicated with a p-value.

If a p-value is listed as less then 0.05, that means that were is less than a 5% chance that a reported

difference is just a fluke finding, and that most likely the results of this study apply to other, similar

patients. Determining “statistical significance” is done with statistical testing, and implies that

distribution of research results match the mathematical models that underscore these statistical tests.

For confidence intervals, a simple test of statistical significance is to see if confidence intervals of risk

ratios or odds ratios overlap. If they do not, there is a high chance that groups have different risks.

One task, however, that statistical significance testing does not perform is to determine clinical

significance. You have to determine that by judging if a reported difference in risk or odds is large

enough to observe clinically, and if it merits changing your clinical practice.

Two other terms you will hear in this course are prevalence and incidence, both of which are measures

of risk for a population of subjects. Prevalence is a measure of how likely a given subject in a population

has a condition or disease, and is simply calculated by the dividing the number of subjects with that

condition over the total number of subjects in a given population.

Incidence is similar to prevalence, but it also includes a temporal component, and it represents the

likelihood of a subject of a given population experiencing a disease or condition within a certain time

span. An example would be the number of flu cases in California between November 2013 and March

2014.

Now that we have reviewed some basic scientific terminology, let us look at nutrition. We will start with

reviewing key nutrients and possible malnutrition states, identify patients at risk for malnutrition and

come up with some strategies of changing nutritional habits to improve oral health.

Macronutrients

When it comes to nutrition, most people will ask, how much do

I need to eat of a certain nutrient to stay healthy? This can be

difficult to answer as different sources will differ on

recommended amounts, and the question on key nutrients can

be obscured by vast quantities of information available.

Although not free of controversy, for this presentation I used

the U.S. Department of Agriculture’s Current Dietary Guidelines

for Americans published in 2015 for recommended amounts of

key nutrients (see Dietary Guidelines for Americans 2015-2020,

8th edition at

http://health.gov/dietaryguidelines/2015/guidelines/ ) .

Generally, these recommendations are accepted as nutritional

guidelines for healthy adults and have good scientific support.

The guidelines are still current until the next version will be

published in 2020, as guidelines usually get updated every five

years.

Generally, the guidelines use the following terminology for

recommended amounts:

The recommended dietary allowance (RDA) is the

recommended average amount of a given nutrient that will be

sufficient for 97-98% of healthy individuals at a given age and

gender to meet nutrition needs. Essentially, this is the daily

amount of a nutrient that a healthy individual needs to

consume in order to stay healthy.

Dietary Reference Intake (DRI) is a new term that replaces the

recommended dietary allowance (RDA) term, and expands it by

including other estimates such as

The adequate intake (AI), which is an estimated average intake of a nutrient as observed in experimental

studies of healthy subjects. The adequate intake is usually reported when a recommended dietary

allowance cannot be determined.

It also includes the tolerable upper intake level (UL), which is the average highest daily level of a nutrient

you can consume while likely having no risk to your health.

LEARNING

OBJECTIVES - RECALL TYPES OF DIETARY

CARBOHYDRATES

- RECALL PURPOSE OF

CARBOHYDRATES IN DIET

- RECALL RELATIONSHIP OF

OBESITY AND PERIODONTAL

DISEASE

- RECALL RELATIONSHIP OF

CARBOHYDRATES AND

CARIES

- ASSESS A PATIENT'S ORAL

HEALTH RISK POSED BY A

PATIENT'S DIET

- RECALL ESSENTIAL AMINO

ACIDS

- RECALL PURPOSE OF

PROTEINS IN DIET

- RECALL DISEASES CAUSED

BY SEVERE PROTEIN

DEFICIENCY

- RECALL PURPOSES OF LIPIDS

IN DIET

- RECALL PURPOSES OF

ESSENTIAL FATTY ACIDS

IDENTIFY BENEFITS AND

RISKS OF CHOLESTEROL,

TRANS-FATTY ACIDS

- ASSESS THE LEVEL OF

EVIDENCE LINKING DIETARY

LIPIDS WITH PERIODONTAL

DISEASE

Before we delve into nutrients and how many miligrams of X you ought to have in your diet, it is

worthwhile to think of why we eat anyway?

Sure, eating can be a source of comfort, pleasure, or can have social functions like a wedding banquet or

a family dinner. But ultimately, we eat to live. Living requires energy, as energy is needed to maintain

orderly processes and structures of life. Every living being requires energy to maintain its cells, to grow,

move about and to store for leaner times.

For this reason, there is a base level of energy needed depending on age and size of the body, with

younger individuals needing more energy for growth, and larger individuals needing more energy. Since

men tend to be larger than women, men also have higher energy needs. (see FDA estimated calorie

needs at http://health.gov/dietaryguidelines/2015/guidelines/appendix-2/#table-a2-1-estimated-

calorie-needs-per-day-by-age-sex-and-physic)

In addition to that basal energy requirement, energy needs increase with increasing amount of physical

activity.

If more energy is created than consumed, energy is stored for future use as glycogen or fat, as a

safeguard against times when there is less food available than required.

Carbohydrates

The primary source for energy is carbohydrates, compounds of carbon, hydrogen and oxygen, arranged

in usually six-member rings of carbon atoms and one oxygen molecule, linked to other rings with oxygen

molecules and hydroxide side chains. Most plants store energy obtained from photosynthesis in the

form of starches, which are long carbohydrate polymers, while in animals the primary carbohydrate

used for energy is glycogen, a large branched carbohydrate polymer. Humans have domesticated wild

grasses for increased grain sizes, and utilize these grains such as wheat, rice and corn as primary source

of carbohydrates. Humans digest these long carbohydrate polymers using salivary enzymes such as

maltose into simpler carbohydrate oligomers and monomers such as maltose and glucose.

Since carbohydrates are vital to life, it is probably the reason why the tongue has taste receptors for

simple carbohydrates on the tip of the tongue in order to find carbohydrate-containing foods. It is

probably also the reason why sweet flavor is generally desirable for humans.

Carbohydrates are largely broken down to the basic 6-carbon sugar glucose, which is largely

metabolized using glycolytic and citric acid cycle into ATP, the body’s basic energy unit, carbon dioxide

and water. If carbohydrate intake exceeds energy needs, glucose will get converted into glycerin, fatty

acids and triglycerides, a.k.a. fat by the liver and stored in adipocytes.

Another use of carbohydrates is a source of precursor multiple carbon units for amino acids and other

molecules synthesized in the body. Glucose units also are extensively incorporated into very large

Figure 2. Fiber intake is related to periodontal status (Staudte et al.

2012). The amount of dietary fiber intake was assessed in 80 patients

with varying levels of periodontal disease, and those patients

categorized as “Periodontitis” and “Control” based on plaque levels,

gingival bleeding and pocket depth. The average fiber intake in both

groups was significantly different (p<0.05).

proteoglycan and glycoproteins that make up the water-retaining and space-maintaining ground

substance proteins of cartilage and connective tissue such as chondroitin and dermatan sulfate.

The RDA of carbohydrates is about 130 grams per day for adults, which equals to just about 5 slices of

bread. Obviously, carbohydrates are found in grains, and grain-based products such as bread and pasta.

Digestible carbohydrates are also found in any fruit, starchy vegetables such as peas and potatoes, milk,

and of course refined sugars, sweets and honey.

Apart from carbohydrates that can be digested by humans, indigestible carbohydrates such as cellulose

are known as dietary fiber. Far from being useless, some amount of dietary fibers is thought to be

important for promoting GI movement and provide moisture retention in stool. Dietary fibers such as

oat bran can also retain cholesterol and prevent high serum cholesterol levels.

In a case-control study by

Dr. Staudte and others

(Figure 2, Quintessence

International 2012; 43:907-

916) of 80 patients, it was

noticed that patients with

periodontal disease had

significantly lower fiber

intake than periodontally

healthy controls. A

drawback of this study is

that “periodontitis” was

merely defined as presence

of pockets greater than 3.5

mm at more than four

teeth, while the healthy

group had to have pockets

equal or less than 2 mm and

no bleeding on probing. This

study suggests that a diet

higher in fiber may be

associated with periodontal

health, but it is unclear if the healthy patients tended to have a healthier lifestyle in general as there

were no smokers in the healthy group compared to the “periodontitis” group.

A deficiency is carbohydrates is rare, but is said to result in loss of energy, being listless, emaciation and

wasting of muscle tissue as muscle protein is metabolized to meet energy needs. Carbohydrate excess in

Figure 3: Israel Kamakawiwo’ole. 450-lb musician

known for his rendition of “Over the rainbow”. Died

of a heart attack and multiple complications from

obesity at age 37.

Table 1: Obesity Classification based on BMI

absence of physical activity will lead to obesity, and by extension of obesity as a risk factor, increase the

risk of type 2 diabetes mellitus, stroke and myocardial infarct. Orally, obesity is associated with

periodontal disease, and excess intake of digestible carbohydrates without proper oral hygiene will

increase the risk of caries.

As mentioned before, obesity is a risk factor

for type 2 diabetes mellitus, coronary heart

disease, hypertension, stroke and myocardial

infarcts. Obesity is also associated with some

cancers of the GI tract, and premature death

as illustrated by musician Israel

Kamakawiwo’ole.

A common screening tool for obesity is the

body mass index (BMI): In order to figure out

a BMI, take a patients weight in kilograms,

and divide it twice by the patient’s height in

meters. If the BMI is greater or equal to 30,

than the patient might be obese. Of course,

this is just a crude screening tool, as well-

built athletes also tend to be considered

“obese” by the BMI. Further observations

and tests such as chest/waist ratio, skin fold

tests and immersion tests are used to arrive at a clinical diagnosis of obesity.

Since obesity is a risk

factor for many chronic

diseases that are costly to

treat, public health

researchers have noticed

with worry that obesity

prevalence in the United

States has been steadily increasing. In California, currently more than 20% of adults are considered

obese (Centers for Disease Control. MMWR 2010; 59:1-5 (early release))

At Western University of Health Science’s Dental Center 13% out of 2,300 patients seen for

comprehensive care were visibly obese, and these obese patients were 1.4 times more likely to have

chronic periodontitis as defined by 1999 International Workshop Definitions. Obese patients also have

more severe periodontal disease than non-obese patients in this clinic. (Figure 4)

What could explain this finding? Mealey and others (2006, Figure 5) proposed a mechanism in their

review of obesity, diabetes and periodontal disease relationships.

We know that periodontal disease is an inflammatory disease triggered by infection of the gingiva.

During the course of this inflammatory process, cells such as neutrophils, fibroblasts and macrophages

release cytokines such as Interleukin-1, Interleukin-6 and Tumor necrosis factor alpha. All of these

cytokines serve to recruit and activate additional immune cells, so that the infection can be contained in

the periodontal tissues. However, as we know, these cells are not successful in eliminating these

bacteria, and the

infection and

inflammatory

process persists.

These inflammatory

mediators, however,

do not stay in in the

periodontium, but

leak into the blood

stream, and get

carried off to other

parts of the body.

Now, one might

think that the

amount of cytokines

released is a trivial

amount since it just

involves a bit of

gingiva next to teeth. However, in a patient with severe periodontal disease, the area of inflammation

has been estimated by Hujoel and Listgarten in 2001 to be 8-20 square centimeters large. 20 Square

centimeters is about the size of your forehead, and so this area of inflammation can be very significant!

Figure 4. Periodontal Disease is more severe in Obese Patients at the Western U Dental Center

1886 Patients were examined between 2010 and 2013 and their periodontal disease diagnosed by

clinical attachment loss. Patients were then categorized according as “visibly obese” if waist width

exceeded chest width, or as “not apparent” if waist to chest ratio appears to be close to unity.

Visibly Obese

Gingivitis

Mild CP

Moderate CP

Severe CP

Health

Obesity not apparent

Figure 5. Mechanism on how obesity influences periodontal disease according

to Mealey BL et al. 2006

The amounts of inflammatory mediators is also significant enough that they can be detected in

meaningful amounts in your serum, and that periodontal disease treatment significantly reduces total

body inflammatory mediators, as shown by d’Aiuto and others in 2004, as well as in a number of other

studies.

We also know now that adipose tissue also uses Interleukin-1, Tumor-necrosis factor alpha, and

Interleukin-6 to regulate fat storage, and the more adipose tissue you have, the higher your systemic

levels of these cytokines are.

So you see that periodontal inflammation and large amounts of body fat can increase your total level of

inflammatory mediators in your body.

Once in the blood stream, tissue does not discriminate where these mediators come from, and the

increased level of mediators will then recruit and activate immune cells throughout the body, enhancing

inflammation throughout the body.

And of course, some of these inflammatory mediators get carried back to the periodontal tissues,

enhancing local inflammation and resulting in even more inflammatory mediators.

Now, inflammatory mediators such as Interleukin 1 and Interleukin 6 also counteract normal insulin

action, preventing uptake of glucose into tissues, presumably so that there is more glucose available for

immune cell function.

Therefore, you increase blood glucose and blood lipids, as the liver will release more glucose and

synthesizes lipids from the higher serum levels of glucose.

Having higher glucose levels in serum also will increase the risk of glucose undergoing a Schiff base

reaction with blood vessel wall proteins, forming advanced glycation end products. These modified

proteins are detected by macrophages throughout the body, and will stimulate these to create more

inflammation and mediators everywhere, including periodontal tissues.

The increased lipid levels are also available to grow more adipose tissue, and increased amounts of lipids

in the blood also increase the potential of these becoming oxidized. These oxidized lipids can damage

blood vessel walls, leading to activation of more immune cells. Ultimately, this proposed mechanism

could explain why obese patients have more periodontal disease, and have a higher risk for developing

type 2 diabetes mellitus, atherosclerosis, hypertension, heart attacks and strokes.

What is the relationship of obesity to periodontitis?

Overall, we can say that there is excellent evidence that periodontitis and obesity are associated, as

summarized in a systematic review by Caffesse and Weston in 2010. Numerous rat studies on obesity,

inflammation and diabetes provide a plausible mechanism as explained before. The only weakness in

our evidence is that there appears to be no study that shows that weight loss reduces periodontal

disease, or that periodontal disease treatment helps with weight loss.

We know however from a cohort study performed by Zuza and others in 2011, that obesity does not

seem to reduce the chance of success for non-surgical treatment of periodontal disease. This at least is

better than tobacco use, which is known to reduce success in periodontal disease treatment.

Since bariatric surgery, also known as “lap band” surgery, is increasingly used to treat obesity, it may be

important to know that in a case series by Moravec and Boyd it was found that bariatric surgery may

adversely affect oral health. Patients who had this type of surgery experienced more gastric reflux,

which could erode teeth, and also developed nutritional deficiencies due to lack of appropriate

counseling and diet change.

When it comes to implants, we do not know of any research that evaluated the effect of obesity on

implants.

What is the relationship between carbohydrates and caries?

We know that caries is associated with an infection of tooth surfaces by acidogenic, meaning acid-

producing, and aciduric, meaning acid-tolerating, bacteria.

It is still not quite clear what causes the onset of caries, but according to Dr. Marsh, caries is the result of

an ecological catastrophe, where changes in the oral environment such as increased presence of

fermentable sugars favors growth of bacteria that are able to ferment these. With time, bacteria that

can ferment sugars will displace bacteria that are protective for the tooth surface, and maintain a new

environment of permanently low pH that favors enamel dissolution and development of clinical caries.

The oral dysbiosis concept proposed by Darveau and Hajishengallis may also apply here as the bacteria

associated with caries are also capable of maintaining their new environment by producing acids and

extracellular matrix which keeps the acid from dissipating.

The classic bacterium associated with caries development is Streptococcus mutans type bacteria, which

are a collection of closely related oral, beta-hemolytic, gram-positive, facultative cocci. They all use

sucrose as a primary energy source, and produce a sticky extracellular matrix composed of glucans using

an enzyme called glucosyltransferase. They also produce lactic acid as a major metabolic byproduct,

which dissolves enamel and causes clinical caries, and along with bacteriocins they produce prevent

growth of other, more protective streptococci.

Xylitol has been shown to inhibit growth of these bacteria by Assev and others in 1983, and it is possible

to prevent caries by patients chewing xylitol containing gum or candy.

While Streptococcus mutans is a prime suspect in caries development, there are many other bacteria

capable of causing caries. Lactobacillus acidophilus, also found in yogurt, produces lactic acid as well and

can survive low pH. It is thought that Lactobacillus may be associated with established caries. Also, other

streptococcal species are also capable of creating caries, especially in animals with teeth other than

humans.

What are cariogenic foods and how can you counsel patients on this topic?

We know that development of caries essentially depends on the balance between fermentable

carbohydrates favoring low pH development and dissolution of teeth, and saliva stimulation and

presence of calcium and fluoride ions in the food, which both favor high pH values and enamel

mineralization.

So depending on the sugar content of the food, and its ability to stimulate saliva or release calcium salts,

food can range from cariogenic, increasing the risk of caries, to preventive, inhibiting development of

caries.

Cariogenic potential also depends on other factors besides overall carbohydrate content. In order to be

cariogenic, the carbohydrates must be able to be broken down to sucrose, glucose or fructose by human

or bacterial enzymes. Therefore, it is mainly foods containing a lot of amylose (starch), sucrose, glucose

or fructose that are considered cariogenic, which means foods such as bread, pasta, rice, candy, cakes,

fruit juices and soda.

In addition, cariogenic potential increases if the food is sticky and does not easily clear from between

teeth, as shown in the Vipeholm studies where chewy candy was given to institutionalized children, who

developed higher rates of caries. Foods that fall into this category are pretzels, potato chips, taffy, sugar-

containing gum, pasta, bread, potatoes, cookies, cakes and similar foods.

Cariogenic potential also increases if cariogenic foods are consumed on a frequent basis, as shown in the

Vipeholm and Michigan studies. This explains why caries risk increases significantly if you sip on juice or

soda throughout the day, but your risk is lower if you restrict cariogenic foods to meal times followed by

oral hygiene.

Therefore, if you have a patient who consumes a lot of sticky, cariogenic foods such as taffy, pretzels,

pasta, white rice, bread, potato chips or chocolate, you will have to watch for caries development. The

same is true for patients who habitually will sip on sodas, fruit juice, sweetened coffee or tea, or hold

hard candy in their mouth. This is also true for children who are fed juice unsupervised in a sippy cup or

nursing bottle.

If you have a patient who experiences more than a few active lesions of caries, you should consider

overconsumption of cariogenic foods as a cause. If the patient is found to overconsume cariogenic

foods, consider the following strategies to limit cariogenic potential instead of simply telling the patient

to quit eating sugary foods:

Try limiting cariogenic foods to the main meal times, in order to decrease frequency of cariogenic food

intake and allow remineralization of tooth surfaces in between meals.

Replace cariogenic snacks with Xylitol-containing gum or candy, or use these products after eating

cariogenic foods to stimulate saliva flow and inhibit bacterial growth. However, advise patients to be

cautious as overconsumption of xylitol can lead to bloating, stomach upset and diarrhea.

Another strategy is to follow cariogenic foods with a drink of water to rinse out sticky foods between

teeth.

Since the pH drops and demineralizes enamel after eating cariogenic foods, tell patients to wait with

brushing and flossing for 30 minutes after eating sugary foods, or rinse out the mouth with water

containing baking soda to neutralize bacterial acids.

You may also suggest replacing cariogenic snacks with foods that favor tooth mineralization:

Vegetables such as carrot, celery sticks, broccoli florets and beans are a nutritious and satisfying

alternative, stimulating salivary flow and food clearance from teeth.

Cheeses are an excellent caries-preventing snack as they provide calcium minerals for remineralization

of tooth surfaces. However, it is important to watch for fat intake as some cheeses can contain a lot of

saturated fats. On the other hand, low-fat varieties might have added carbohydrate content to make

them feel smooth in the mouth, and some carbohydrates might be cariogenic. The best cheese snacks

might be string cheese sticks, or strongly flavored hard cheeses such as Parmesan or feta cheese where

small amounts are quite satisfying.

Nuts are also a good satisfying snack that supplies energy. However, nuts may be contraindicated in a

patient with brittle teeth or fragile restorations.

For some patients, a good alternative to a solid snack is a glass of skim milk, tea without sugar or water,

either plain or flavored with sugar-free additives. As added benefit, green and black tea contain fluoride,

but can also stain teeth.

What is the level of evidence behind all these recommendations?

Given the focus of dentistry on caries, what is the level of science behind nutrition recommendation?

On one hand, it is a very well researched field, and we know from several long term cohort studies such

as the Michigan, Vipeholm, Newcastle/Northumberland studies that caries is associated with increased

frequency, amount and stickiness of consumed cariogenic foods. We also have decades of benchtop

research demonstrating mechanisms of caries on bacterial cultures, extracted teeth, dentin disks and in

various animals.

However, we still do not know conclusively if caries can be reduced by reducing sucrose intake, as a

systematic review by Stillman-Lowe and others in 2005 failed to produce conclusive evidence.

So, it is a good idea to look into a patient’s diet as a possible etiology of current caries experience.

However, reduction of cariogenic foods alone may not be enough to reduce a patient’s caries

experience. In a patient with significant amounts of caries you should also consider evaluating quantity

of saliva, pH and buffering capacity of saliva; amounts of cariogenic bacteria; mucogingival, restorative

and anatomic factors favoring plaque retention; occlusal function; parafunctional habits and medical

history to investigate causes of caries in these patients.

For management of patients with high risk or incidence of caries, you should consider caries

management by risk assessment techniques as developed by University of California at San Francisco,

also known as CAMBRA. A course in CAMBRA methodology is currently available for free on the

California Dental Association’s website at www.cda.org.

Proteins and Amino Acids The next important macronutrient is proteins or amino acids. Proteins are digested in your duodenum

into amino acids for absorption in the small intestine. Humans use twenty two amino acids for synthesis

of proteins, which could be either structural such as collagens found in bone, periodontal ligament or

teeth, or have other functions such as enzymes, antimicrobial peptides or antibodies.

As an alternative energy source to glucose, amino acids can be metabolized to yield energy, although at

lower efficiency.

For humans, there are nine essential amino acids that the human body cannot synthesize in sufficient

quantities on its own, and that are needed in the diet to maintain health. These are histidine, leucine,

isoleucine, lysine, methionine, phenylalanine, threonine and valine. Tryptophan is also considered an

essential amino acid since the body can only synthetize limited amounts of it from phenylalanine.

The RDA of protein is 0.6 of protein per kg bodyweight. So, for a dental student weighing 150 lb, the

average protein requirement for the day is only a little less than a two-ounce filet mignon, which is likely

less than the smallest steaks served at any restaurant.

To put this in context, the US Department of Agriculture estimated that in 2000, the average American

ate 195 pounds of meat in the year, or about 8 ½ ounces per day. This is also the reason why total

protein deficiency and deficiencies of specific amino acids are quite rare.

During famines, protein deficiency may manifest itself in a severe form

called Kwashiorkor disease (Figure 6), producing muscle wasting and

bloated abdomen from increased fluid retention in the peritoneal

cavity, and the condition is eventually fatal. More commonly, protein

deficiency will result in stunted growth and development of children,

and poor wound healing and risk of infections. Since wound healing is

impaired and resistance to infections lowered, periodontal disease

may become severe in patients with protein deficiency, and

necrotizing periodontal diseases culminating in Noma or facial

gangrene can develop.

Protein deficiency to this extreme is unlikely encountered in a

common dental office, as proteins are widely available in meats, dairy,

legume such as kidney beans, eggs and to a lesser degree in most

other foods.

Figure 6. A 3-4 year old boy

suffering from Kwashiorkor

(J.E. Armstrong)

Lipids The third important macronutrient is fat. According to USDA guidelines, fats should make up 25-35% of

caloric intake, which sounds like a lot, but actually is easily achievable given the high calorie content of

fat. The USDA recommends eliminating solid fats as much as possible, aiming for a level of less than

10% of caloric intake, or about ½ ounce per day. Most fats consumed should be in the form of liquid oils,

or a little less than one ounce per day.

Lipids get digested as they get emulsified into small droplets by bile liquid and absorbed in the small

intestine, producing chylomicrons that are further processed by the liver into packages of Very low

density lipoprotein (VLDL) and low density lipoprotein (LDL) for further consumption in body tissues.

Fats are mostly needed as energy source and for energy storage, but are also important part of organs

and form a protective, insulating layer around vital organs. Fats are also used for absorption of fat-

soluble vitamins, and serve as major component of cell membranes and cell organelles. Important

hormones and immune mediators such as androgens and prostaglandins are synthetized from certain

fats.

There are two essential fatty acids needed in human diet, both of them unsaturated cis-fatty acids found

in plant oils and certain animals.

One is linoleic acid, with an adequate intake level of about 12-17 grams per day, and mostly found in

vegetable oils such as safflower, grape seed, corn and to a much lesser degree, olive oil.

The other essential fatty acid is either alpha linolenic acid (ALA), Eicosapentaenoic acid (EPA) or

Docosapentaenoic acid (DPA), which can be interchangeably converted by the body. The adequate

intake level is about 1.1 to 1.6 grams per day for ALA, and they are found in cold water marine fish oil,

kiwifruit or flax seeds.

Both essential fatty acids are needed as precursors for arachidonic acid, an important precursor for a

variety of messenger molecules such as prostaglandins. Linolenic acid (ALA) and related acids are called

n-3 fatty acids, and converted slower to arachidonic acid, which supposedly results in an anti-

inflammatory effect as prostaglandin synthesis is slowed down.

The reason the USDA is emphasizing using predominantly oils as a fat source is that liquid oils contain

unsaturated fatty acids including essential fatty acids, whereas solid fats are made of saturated fatty

acids that are solid at room temperature. Solid fats can also be generated by hydrogenating vegetable

oils, which converts unsaturated fatty acids into saturated fatty acids by adding hydrogen atoms to

double-bonded carbons.

Since this process involves heat, it can also produce what is called trans-fats such as elaidic acid. Trans-

fats develop when naturally occurring oils are heated, which causes the cis-configuration double bonds

to be transformed into trans-forms.

Trans-fats are desirable from a food manufacturing point as they are cheap, have higher melting points

than normal vegetable oils, and make products containing trans-fats chewier, moister, softer and more

stable while being stored.

Unfortunately, trans-fats are not easily metabolized, and increased intake of trans-fats has been

associated with higher LDL, triglyceride levels (Katan MB et al. 1995); increased systemic inflammation

(Mozaffarian D et al. 2004); higher risk of cardiovascular disease and diabetes (Ascherio A et al. 1999;

Salmeron J et al. 2001).

Therefore, since about the mid-2000s, use and consumption of trans-fat containing foods has been

discouraged.

Cholesterol received a bad name in the 1990s when the relationship of heart disease and high

cholesterol levels became publicized. However, small amounts of cholesterol less than 300 mg per day

are needed as cholesterol forms a vital part of cell membrane, where it stabilizes the cell membrane,

preventing cell death.

It is found in any animal products as all animal cells contain cholesterol, but it is especially common in

egg yolk, liver and shellfish.

What is the relationship between lipid intake and periodontal disease?

Interestingly, in a Chinese study by Shi D and others (2006), patients with aggressive periodontitis and

chronic periodontitis had significantly higher levels of serum cholesterol than those who had gingivitis or

periodontal health.

A year later, a randomized clinical trial by Oz SG and others (2007) demonstrated in fifty patients that

serum LDL and cholesterol significantly decreased in three months if subjects had non-surgical

periodontal treatment.

Judging from several mice experiments, small clinical trials and larger cross-sectional studies, it seems

that intake of unsaturated fatty acids may be beneficial for periodontal disease. Bendyk A and others

(2009) noted that in experimental periodontitis mouse model, omega-3 fatty acid supplementation in

the mice’s diet was associated with less bone loss. There are also similar Japanese studies on rats

confirming this observation.

In humans, Naqvi AZ and others (2010) analyzed data from the 1999 to 2004 National Health and

Nutrition Examination Survery (NHANES), and found that adults who had higher dietary levels of n-3

fatty acids had less periodontitis. Similarly, a diet with low n-3 fatty acid content was associated with

higher levels of periodontitis in a survey of older Japanese (Iwasaki M et al. 2001).

Interestingly, Rosenstein ED and others (PLFA journal 2003; 68(3):213-8) conducted a small clinical trial

where they treated small groups of patients with scaling and root planing and different fatty acid diet

supplements. The found that borage oil, a plant oil rich in n-6 fatty acids showed significant reduction in

inflammation and pocket depths (about ½ mm) compared to patients who took placebos or other types

of oils in 3 months. (Table 2) It was also interesting to see that fish oil, a source of n-3 fatty acids, and

shown to be associated with less periodontal disease in the Japanese study mentioned before had no

effect. Findings from this study were confirmed by another study by Deore and others in 2014, with

similar methodology and similar results.

Table 2. Dietary fatty acid supplementation influenced periodontal

treatment outcomes

Adult patients received fatty acid supplements for 12 weeks after

scaling and root planning, and periodontal parameters were

measured before and after this time period.

Micronutrients - Vitamins

As important as the macronutrients in your diet are

micronutrients such as vitamins, as their name suggests “vita”,

Latin for life.

Fat-soluble Vitamins

Vitamins can be classified as either fat-soluble or water-soluble.

The vitamins A, D, E and K are fat-soluble.

Vitamin A

The dietary reference intake for vitamin A is 900 micrograms or

3000 international units for men and 700 micrograms for

women. Vitamin A has two important functions. One is a role in

cell differentiation and maturation, for example during tooth

development. The other important function is its role as

precursor to retinal pigment, where it is essential for night

vision. Vitamin A can be consumed in two varieties in a diet.

One is as retinoids, a group of closely related chemicals found

in animal fats and especially fish oil. The other variety is plant-

derived carotenoids which your body can convert into retinoids

as needed. As the name suggests, carotenoids are found in

carrots, but also in many other darkly colored leafy vegetables

or red/orange colored vegetables such as cantalopes and bell

peppers. Unlike retinoids, carotenoids are not toxic, and can

serve as anti-oxidant.

As Vitamin A is essential for retinal pigments, deficiency will

result in blindness. It also leads to impaired brain function, and

development abnormalties.

As hinted at before, retinoids are toxic at high doses, and a

retinoid overdose will result in dry mouth, loss of hair and headaches. Vitamin A toxicity may also

produce gingival erosions, ulceration, bleeding, tissue swelling and dekeratinization of gingiva.

There is no known relationship of vitamin A levels and periodontal disease, but since Vitamin A supports

cell differentiation case reports of Vitamin A improving drug induced overgrowth (Norris JF & Cunlifee

WJ 1987), lichen planus (Piatelli A et al. 2007) and leukoplakia (Epstein JB & Gorski M 1999) seem

plausible.

LEARNING

OBJECTIVES - RECALL FAT SOLUBLE

VITAMINS

- RECALL CONSEQUENCES OF

DEFICIENCIES IN FAT-

SOLUBLE VITAMINS

- RECALL SOURCES OF FAT-

SOLUBLE VITAMINS

- RECALL CONTRIBUTIONS OF

FAT-SOLUBLE VITAMINS TO

ORAL HEALTH

- RECALL DEFICIENCY STATES

CAUSED BY B-VITAMIN

DEFICIENCIES

- RECALL SOURCES OF B-

COMPLEX VITAMINS

- RECALL GENERAL ROLE OF

B-COMPLEX VITAMINS

- RECALL RELATIONSHIPS OF

B-COMPLEX VITAMINS WITH

PERIODONTAL DISEASE

- RECALL FUNCTIONS OF

VITAMIN C

- RECALL DEFICIENCY STATES

CAUSED BY VITAMIN C

DEFICIENCY

- ASSESS THE LEVEL OF

EVIDENCE LINKING VITAMIN

C WITH PERIODONTAL

DISEASE

Vitamin D

Vitamin D is another fat soluble vitamin, and the metabolically active form is calciferol or vitamin D2.

The dietary reference intake level is 15 micrograms per day or 600 international units, and the main role

of vitamin D is calcium metabolism. It promoted calcium uptake from the intestines, maintains adequate

calcium serum levels and promotes bone turnover and calcification.

Main dietary sources are fortified milk and cod liver oil, but in sunny climates, fair-skinned humans make

sufficient vitamin D in skin tissue if exposed 15 minutes a day to sun light.

Vitamin D deficiency will result in either osteomalacia in adults or Rickets in children. In children, where

bone still develops, Vitamin D deficiency will result in deformed bones as mineralization is delayed,

creating bowed legs and deformed chest cavities, known as rachitic chest. In adults, growth is complete,

but vitamin D will impair bone turnover and adaptation to mechanic stress, resulting in increased risk of

fractures and bone pain.

Overdoses of vitamin D will result in too high serum calcium levels, which will produce abdominal

cramps and vomiting, as well as cardiac arrhythmia, confusion, and ultimately death.

If there is a chronic, but slight overdose of vitamin D, there is an increased risk of kidney stones.

Unlike Vitamin A, Vitamin D may play a role in periodontal disease given its role in bone metabolism.

Dietrich and others found in NHANES data a positive association of high Vitamin D levels and periodontal

health (Dietrich et al. 2004, 2005), while Bogess and others found low levels of Vitamin D associated

with periodontal disease in pregnant women (2010).

Interestingly, Bashutski

and others (Figure 7, J

Dent Res 2011;

90(8):1007-12) performed

a clinical trial with

patients who either had

low serum Vitamin D

levels or high levels. For

these patients they

performed flap surgery for

pocket reduction and

noted that patients with

sufficient serum Vitamin D

levels had consistently

lower pocket depths after

surgery and greater

attachment gain

compared to patients with

Vitamin D insufficiency.

So, it might be useful to

supplement patients

undergoing periodontal

surgery with Vitamin D if

Vitamin D levels are

suspected to be low.

Figure 7. Vitamin D improves outcomes after periodontal pocket reduction

surgery in Vitamin D – deficient patients.

Periodontal disease parameters in the months following flap surgery on

Vitamin D-deficient patients who either received placebo or Vitamin D

containing supplements.

Vitamin E

Vitamin E is a group of 8 lipid-soluble chemicals called tocopherols, and their main function is to be

scavenger molecules that prevent oxidative damage to cell membranes.

The dietary reference intake is 15 milligram, and it can be found in nuts, seeds and whole grains, as well

as spinach.

Vitamin E deficiency is rare, but it may produce ataxia, meaning the inability to walk, and peripheral

neuropathy.

There is no toxicity syndrome, but there have been case reports of patients who took mega doses of

vitamin E and having bleeding complications. Through some mechanism, vitamin E seems to interfere

with clotting mechanisms (Dowd D & Zheng ZB 1995).

The relationship of Vitamin E and periodontal disease is unclear, since a study showed a slight

association of serum Vitamin E to attachment loss (Iwasaki M et al. 2012), but other studies did not

show a relationship or improved treatment outcome with vitamin E deficiency (Carvalhorde S et al.

2013; Slade EW Jr et al. 1976; Cohen RE et al. 1991)

Vitamin K

The last fat-soluble vitamin, Vitamin K, is an important cofactor for enzymatic carboxylation of glutamic

acid residues. As such it is required for synthesis clotting factors II, VII, IX and X, and it is also required

for bone proteins suchas osteonectin and bone-matrix gla proteins.

The dietary reference intake is 120 microgram for men, and 90 microgram for women, and it is mainly

found in dark green leafy vegetables such as spinach, romaine lettuce and broccoli. Intestinal bacteria

also produce a significant amount of vitamin K.

As you would expect, vitamin K deficiency results in a hypocoagulative state similar to that induced by

Coumadin or Warfarin, and reduced bone mineral density.

Vitamin K toxicity is rare, but can occur in infants who received vitamin K injections after birth and who

get vitamin K-supplemented formula after birth. Similarly, patients who receive regular injections of

Vitamin K might get this condition. In this case, jaundice develops from hemolytic anemia, producing too

much bilirubin that discolors the skin.

There is no known effect of Vitamin K on periodontal disease.

Water-soluble Vitamins

The water-soluble vitamins are either part of the B complex or vitamin C. As water-soluble vitamins,

they all have fairly low toxicity as the body tends to excrete excess vitamins in urine. However, because

of the same property, water soluble vitamins usually are not stored in the body, and deficiency states

are more common. All vitamin B complex vitamins are associated with some metabolic function. The

term vitamin contains “amin” since many B complex vitamins contain carbon-nitrogen bonds like the

chemical class of amines.

Vitamin B 1 (Thiamine)

Thiamine is typical of the vitamin B complex that it contains these chemical structures and is involved in

metabolism and energy production. The dietary reference intake is 1.1 to 1.2 milligram per day, and it is

found in a variety of foods ranging from fortified breakfast cereal to meats and orange juice.

Alcoholics or patients with gastric bypass surgery and inadequate dietary counseling may experience

Beriberi deficiency. Beriberi disease got its name from a Sinhalese word meaning “extreme weakness”,

and may date back to times when unfortified white rice was a staple food and meat rare, causing

thiamine deficiency. There are two varieties of this disease: One is dry beriberi, where there is a gradual

degeneration of peripheral nerves and muscles in legs and arms, causing weakness and eventual

inability to support oneself. The more acute version of the disease, wet beriberi, there is edema as a

result of cardiac insufficiency. Onset of symptoms can be quite fast within a week or so of a diet lacking

thiamine, but recovery depends on the type of symptoms encountered. Cardiac symptoms tend to

improve quickly with thiamine supplementation, whereas nerves take much longer to recover, of if

severe, will never recover.

In alcoholics, thiamine deficiency may also be associated with Wernicke-Korsakoff Syndrome that

produces slowing of conscious movement, nystagmus, ataxia, and eventually loss of consciousness and

death. In some, it can also cause mental confusion, dysphonia, meaning blurred and unintelligent

speech, and confabulation, or the making up of events and stories.

Vitamin B complex may be associated with periodontal health as some B-vitamins were associated with

longer retained teeth in elderly Japanese (Yoshihara A et al. 2005), and a small randomized clinical trial

by Neiva and others (Table 3, Journal of Periodontics 2005) with patients undergoing pocket reduction

surgery showed s a small improvement in attachment level if the patients had taken vitamin b complex

supplements. Best improvement was observed with deep pockets, where almost an additional

millimeter of attachment gain was observed.

Vitamin B 2 (Riboflavin)

Riboflavin, or Vitamin B2, functions as electron recipient during energy production, and is needed 1.3

milligrams per day. It can be found in milk, fortified breakfast cereals and any animal products.

There is no known deficiency state or toxic state, or any effect known on periodontal health. It has been

suggested in some textbooks that riboflavin deficiency may result in glossitis, angular cheilosis and

stomatitis, but I could not find any case reports supporting this statement.

Vitamin B 3 (Niacin)

Niacin, or Vitamin B 3, is involved in a multitude of metabolic processes, and plays a role in fat and

energy metabolism. The dietary reference intake value is 14 to 16 milligrams per day, and again found in

fortified breakfast cereal. It is also found in a variety of other foods such as beets, yeast, organ meat,

fish, seeds and nuts. The body can also synthesize small amounts from tryptophan, as the similar

chemical structure suggests.

As with thiamine, the main risk factor from deficiency in this country is alcohol abuse. Niacin deficiency

results in a condition called Pellagra (Figure 8), which produces the following signs, referred to as the “4

Ds”, in the sequence they occur with increasing severity of the niacin deficiency: Dermatitis, Diarrhea,

Dementia and Death.

Table 3: Vitamin B complex supplementation improves outcome after periodontal flap surgery

(Neiva BL et al. 2005)

Parameter Group Baseline 90 days 180 days Change

PD Vit-B 3.98+-0.57 2.47+-0.16 2.41+-0.23 -1.57+-0.34

Placebo 4.32+-0.56 2.50+-0.30 2.82+-0.35 -1.50+-0.21

CAL Vit-B 4.03+-0.94 3.86+-0.80 3.62+-0.82 +0.41+-0.12*

Placebo 4.07+-1.14 4.33+-1.22 4.59+-1.39 -0.52+-0.23

Both groups significantly improved after periodontal flap surgery; however the group receiving

Vitamin B supplementation had significant gain of attachment compared to the placebo group.

Uncommon for water-soluble vitamins, niacin exhibits some

toxicity at doses of 0.7 to 1.6 grams, which is only attainable by

ingesting niacin supplements. As niacin has cholesterol lowering

properties, some patients used it as a “natural” anti-cholesterol

drug, and ended up with toxicity, mostly involving a flushed and

itchy skin. At extreme doses, it can induce nausea and liver

damage.

Vitamin B 4 (Choline)

Choline was once called vitamin B4, but is not essential.

The daily reference intake for choline is about 550 milligrams per

day, and as part of phosphatidylcholine it is an important structural component of cell membranes.

Phosphatidylcholine, which is the major component of lecithin, is also part of an important membrane

lipid cell signaling system performing numerous tasks. It also plays an important role in transmission of

nerve impulses, methyl transfers, lipid transport and metabolism.

Choline is found in fatty foods such as milk, egg, liver and peanuts.

Choline deficiency is rare in healthy humans since normal diet usually contains some choline, and the

majority of needed choline can be synthesized in the body. In patients unable to eat, choline deficiency

may appear and cause fatty liver and hyperlipidemia, demonstrating its role in lipid metabolism.

The upper intake limit appears to be about 3.5 milligrams per day, and there is no known effect on

periodontal disease.

Vitamin B 5 (Pantothenic Acid)

Vitamin B5, or much more commonly called Pantothenic acid, is a component of co enzyme A, and thus

responsible for synthesis and breakdown of fats, cholesterol, steroid hormones, acetylcholine and

melatonin. Co-enzyme A is also involved in maintaining the citric acid cycle for energy production.

The dietary reference intake value is 5 milligram per day in adults, and it is found in many foods.

As it is found in many foods, deficiency is rare, possibly producing paresthesia and dysesthesia in feet.

There is no known toxicity syndrome. In a cross-sectional study of older Japanese, persons with low

levels of pantothenic acid had more periodontal disease (Yoshihara A et al. 2005)

Figure 8. Sharply Delineated

dermatitis on sun-exposed skin (from

Robbins & Coltran Pathologic Basis of

Disease, 7th edition)

Vitamin B 6

Vitamin B6 is a group of similar chemicals involved in many metabolic reactions ranging from nucleic

acid synthesis to amino acid synthesis and lipid metabolism. The dietary reference intake is 1.7 milligram

per day, and again it can be found in many foods such as nuts, fortified breakfast cereal, fish and

poultry, bananas and spinach.

Vitamin B6 deficiency is rare, but may result in seizures. On the other hand, Vitamin B6 also has nervous

system toxicity at very high doses in excess of 200 milligram per day.

Again, as with several other B complex vitamins, vitamin B6 deficiency may be associated with

periodontal disease. (Yoshihara A et al. 2005)

Vitamin B 7 (Biotin)

Biotin, or rarely called vitamin B7, is needed for carboxylase enzymes to function. It also is needed for

energy storage and production, leucine metabolism, metabolism of odd chain fatty acids and

biotinylation of histones where it controls DNA transcription and replication

The dietary reference intake value is small at 30 microgram per day, and it is found in many foods. Gut

bacteria may also synthetize it.

Since it is found in many foods, deficiency is rare, but it is speculated to involve hair loss, a scaly red rash

and various neurologic symptoms such as hallucination and paresthesia.

There is no known toxic level, and no association with periodontal disease.

Vitamin B 8 (Inositol)

Inositol, or Vitamin B8, is not known to have deficiency or toxic states, and some users take grams of

this substance for support against anxiety disorders. It is widely found in foods and there is no known

periodontal or oral health effect of this vitamin.

Vitamin B 9 (Folic acid, Folate)

Folic acid, or folacin and rarely called vitamin b9, is required for thymidine synthesis and amino acid

metabolism. The dietary reference intake is 400 micrograms per day, and it can be found in fortified

cereals, poultry, fish, spinach, beans and many other foods.

Since folic acid is quickly destroyed by heat, cooked food contains low levels of folic acid. In adults,

severe folic acid deficiency will result in megaloblastic anemia. Folic acid is critical in early neuronal

development, and is given to pregnant women to prevent neural tube defects such as spina bifida.

There is no known toxicity.

Folic acid may be protective for periodontal disease, as Dr. Yu YH and others (2007) noticed in NHANES

data that adults with low levels of serum folate will have higher levels of periodontitis. Similarly, Staudte

and others (2012) noted that for a small sample of German individuals.

Interestingly, two small randomized clinical trials demonstrated that folic acid supplementation reduced

phenytoin- induced overgrowth in children (Arya R et al. 2011; Brown RS et al. 1991)

Vitamin B 10 & B 11

Vitamin b10, which is more widely known as para-amino benzoic acid, and vitamin b11, which is salicylic

acid, are not recognized as vitamins by the USDA, but used as dietary supplements as shown here. There

is no known need or toxicity, but some alternative medicine sources suggest these being useful for a

variety of conditions. Salicylic acid is related to acetylsalicylic acid, or aspirin, and also has similar effects

on pain, fever and platelets. 6% Salicylic acid is most commonly used in cosmetic and anti-dandruff

products as it exfoliates skin and kills skin bacteria. It is also used as food preservative in small amounts.

Dietary supplement sites list salicylic acid as not having toxic effects, but that is incorrect as high doses

of salicylic acid in excess of 150 mg/kg cause metabolic acidosis.

Vitamin B 12 (Cyanocobalamin)

Vitamin B12 or cyanocobalamin is involved in one carbon unit transfers, and essential to regenerate folic

acid during thymidine synthesis. The daily recommended intake is 2.4 microgram per day for adults,

with older adults needing more.

It is only found in animal sources, and is the one supplement that vegans must take in order to avoid

megaloblastic anemia.

During pernicious anemia, Vitamin B12 uptake is impaired as the cells making intrinsic factor required

for Vitamin B12 uptake are destroyed during an autoimmune reaction. As consequence, Vitamin B12

deficiency is the result, which leads to development of megaloblastic anemia, and it may also produce

numbness, ataxia and death depending on the severity of the condition. The is no known toxicity and no

known effect on periodontal disease

Vitamin C (Ascorbic acid)

Vitamin C is ascorbic acid, and its main function is to help hydroxylation of proline and lysine for collagen

synthesis. It also is an energy source for neutrophils and macrophages, and is found in vegetables and

fruits such as citrus fruits.

Deficiency is rare, but possible with a diet poor in fresh vegetables and fruits. The classic deficiency

syndrome of vitamin C is scurvy, which produces muscle weakness, lethargy, diffuse tissue bleeding and

bruises, painful and swollen joints, gingivitis and loosening of teeth. Rebound scurvy can happen in

patients who regularly take large doses of vitamin C and suddenly stop taking it.

Vitamin C insufficiency might also be associated with unusually severe periodontitis.

Toxicity is expected at a level greater than 1 gram a day, and probably results in kidney stones.

Surprisingly, the evidence linking vitamin c to periodontal health is quite weak, as all studies only show

small differences and are limited to either animal studies or cross-sectional studies. (Nishida et al. 2000;

Tomofuji et al. 2006; Iwasaki M et al. 2012; Staudte H et al. 2012)

There is no compelling evidence at this point that vitamin c mega doses improve immune function.

Micronutrients – Electrolytes and Others

Besides vitamins, there are a number of minerals that are

essential to life. Some minerals are needed in large quantities,

whereas some other minerals are needed only in trace

amounts.

Sodium Sodium ion is the most common positively charged ion in

extracellular fluid, and is a key electrolyte involved in fluid

retention and nerve conduction. The optimum intake is 0.5 to

2.4 grams per day, depending on perspiration, but the average

intake for most adults is higher than that. Sodium ions are

found in any food, but of course concentrated in salt, canned

vegetables and other processed foods.

Deficiency is rare, but can happen as a result of dehydration or

excessive water consumption, diarrhea or vomiting, and

produces a medical emergency called hyponatremia. Major

electrolyte imbalances such as hyponatremia usually start with

headaches, progresses to confusion, seizures and ultimately

death.

There is no known toxic syndrome, but excess intake of sodium

ions has been associated with hypertension.

There is no known effect on periodontal disease, also warm salt

water rinses can help healing after surgery.

Potassium Potassium ion is the most common positively charged ion inside

of cells, and has similar functions like sodium, but INSIDE cells.

Potassium levels are associated with decreased blood pressure

and stroke risk.

There is no recommended amount, but is estimated that 1.6 to 3.5 gram per day is adequate. Potassium

ions are found in most foods, but particularly in foods such as oranges, prunes, bananas, strawberries,

watermelons, mushrooms, leafy vegetables and most types of meat.

Potassium deficiency is rare, but can be caused by loop diuretics. Hypokalemia is another medical

emergency, manifesting itself with muscle cramps, confusion, cardiac arrhythmia and death.

LEARNING

OBJECTIVES - RECALL FUNCTIONS OF

MAJOR ELECTROLYTES

RECALL DEFICIENCY AND

TOXIC STATES OF MAJOR

ELECTROLYTES - RECALL EVIDENCE LINKING

ELECTROLYTES WITH

PERIODONTAL DISEASE - RECALL ROLE OF SULFUR

AND PHOSPHOROUS - RECALL ROLE OF IRON IN

METABOLISM - RECALL ROLE OF ZINC IN

METABOLISM AND

DEFICIENCIES - RECALL HALIDE

DEFICIENCIES AND SOURCES

OF THESE IONS - RECALL OPTIMUM WATER

FLUORIDATION LEVEL - RECALL THE ROLE OF

SELENIDE, COPPER,

CHROMIUM, MANGANESE

AND MOLYBDENUM IONS IN

METABOLISM - RECALL TRACE MINERALS

THAT MAY HAVE A

BENEFICIAL EFFECT ON

PERIODONTAL DISEASE

Toxicity is rare, but excess serum potassium can happen as result of extensive tissue damage or

Addisons disease, in which case nausea, bradycardia or cardiac arrhythmia could result from this

condition.

There is no known effect on periodontal disease.

Magnesium

Magnesium is the second most common positive ion inside cells, and it is involved in energy transfers

and enzyme function. Dietary reference intake is 420 mg, and it is found in many foods.

Hypomagnesemia can occur in alcoholics and frequently in ICU patients, with more than half possibly

affected. Hypomagnesemia will result in cardiac arrhythmia, disorientation, combativeness, psychosis,

ataxia, vertigo and ultimately death.

The role of magnesium in heart physiology is exemplified by the fact that a severe, life-threatening form

of polymorphic ventricular tachycardia called “torsade de pointes” can sometimes be reversed with an

infusion of a large amount of magnesium salts.

Hypermagnesemia is rare, and usually caused by renal failure, lithium therapy or Addison disease. The

consequences of hypermagnesemia are muscle weakness, loss of tendon reflexes and bradycardia.

There several cross-sectional studies of small patient populations that shown an association of

magnesium with periodontal health (Meisel et al. 2005; Tanaka K et al. 2006; Staudte H et al. 2012)

Calcium

Calcium ion is the primary positive ion of hard tissue mineralization, and involved in muscle contraction.

The dietary reference intake is 1.3 grams/day, and it can be found in dairy, calcium-enriched foods,

canned fish and various vegetables such as soybeans and collard greens.

As with all electrolytes, calcium deficiency can be life threatening if severe, and calcium insufficiency is a

risk for osteoporosis.

It is important to know that calcium supplements and dairy products can interfere with absorption of

many drugs such as tetracyclines, vitamins and ciprofloxacin. Excess intake of calcium can result in

nausea and constipation.

As calcium is related to bone metabolism, several studies have investigated a possible role in

periodontal disease. Unfortunately, the evidence is inconclusive, as an older study Uhrborn E and

Jacobson L (1984) did not show any effect of calcium supplementation. Newer studies do seem to show

an association between calcium and periodontal health, however the evidence is quite weak. (Krall et al.

2001; Miley et al. 2009; Adegboye AR et al. 2012)

The highest level of evidence of a role for Vitamin

D and calcium supplementation is a moderately

sized cohort study of about 120 patients, half of

which take Vitamin D and calcium supplements

and the other does not. In that study, Garcia and

others noted during 1 year of periodontal

maintenance that subjects who took Vitamin D and

Calcium supplements consistently had better

clinical characteristics to begin with, and had

slightly better periodontal maintenance outcome

throughout the study (Figure 9). It is unclear

though if the subjects taking these supplements

also had better eating and hygiene habits overall.

Chloride

Chloride is the major negative ion

counterbalancing potassium and hydrogen ion, and

is important for nerve and muscle function. The

Bohr effect in erythrocytes regulating hemoglobin

oxygen binding also depends on chloride ions.

Chloride ions are found in all foods, and there is no

known deficiency in adults or role in periodontal

disease.

Phosphorus

Phosphorous as phosphate and related ions are important for nucleic acid synthesis, but also as pH

buffer and for energy transfers. Phosphate ions are the major counterbalancing ions to calcium in hard

tissues, and the dietary reference intake value is 700 milligram per day.

There is no known deficiency, toxicity or role in periodontal disease.

Sulfur

Unlike the previous minerals, sulfur is found in both organic and inorganic molecules. It is part of

cysteine and methionine amino acids, and at the active sites of co-enzymes such as co-Acetyl and

Figure 9. Patients attachment levels tend to be

better if patients take Vitamin D and Calcium

supplements.

Patients received periodontal therapy and

maintenance for 1 year. Mean attachment level

was always significantly better in patients who

used Calcium/Vitamin D supplements (light blue)

compared to patients who did not (purple)

glutathione. It also is a major negatively charged ion attached to heparin and chondroitin. There is no

known deficiency syndrome or role in periodontal disease.

Patients may have allergies to sulfites or sulfonamides.

Iron Iron has two oxidative states, with ferrous iron being the preferred ion. Ferric ion is toxic to cells. The

dietary reference intake value is 18 milligram per day for adults, and iron plays an important function in

oxygen transport in hemoglobin, and redox reactions. Red meat and red grapes are an good sources of

iron.

Iron deficiency will produce hypochromic anemia, whereas iron overdose will cause liver cirrhosis. There

is no known role in periodontal disease.

Zinc

Zinc ions are cofactors for more than fifty enzymes, and the dietary reference intake is 11 miligram/day

for adults. Zinc ions are found in most foods, and it is thought that zinc deficiency produces impaired

wound healing, mild anemia and short stature.

Given its role in wound healing, there was some interest in studying a relationship between zinc and

periodontal disease. Unfortunately, some studies show a positive association between zinc and

periodontal health (Orbak R et al. 2007; Willershausen B et al. 2011) while others don’t. (Freeland JH, et

al. 1976; Tanaka H et al. 2006)

Iodide

The only role of iodide ions is to be part of thyroid hormones, which control the rate of metabolism. The

dietary reference intake is 150 micrograms per day, and iodized salt or ocean fish are good sources for

iodine. Strangely enough, deficiency and overdose will induce goiter formation, enlargement of the

thyroid gland. There is no known role of iodine in periodontal disease.

Fluoride

Fluoride ions are needed in small amounts to support tissue mineralization, and the adequate intake

level is estimated to be 0.03 to 0.05 milligram per kilogram. Fluoride naturally occurs in sardines, grapes

and green or black teas, and can also be obtained through drinking fluoridated water, or using

fluoridated salt or infant formula.

Fluoride deficiency increases the risk of caries and osteoporosis, while levels greater than 5 mg per

kilogram will induce toxic reactions such as nausea, vomiting, diarrhea, abdominal pain and paresthesia.

As an added note, stannous fluoride has antibacterial properties.

The optimum water fluoridation level is 0.7 to 1.2 parts per million, with fluoridation levels decreasing

for hotter climates to counteract increased water consumption.

The environmental protection agency has set a maximum level of 4.0 mg/L or 4.0 parts per million for

drinking water, and it estimates that undesirable side effects such as dental fluorosis happen at levels of

2.0 parts per million and above.

Selenium

Selenium, or to be precise, selenide ions, is another micronutrient that is toxic at high amounts, but

required at low amounts. The dietary reference intake value is 55 micrograms per day for adults, and

selenide is required to maintain the glutathione peroxidase system, which protect cell and cellular

organelle membranes from oxidative damage. It is thought that a deficiency in selenide lowers

resistance to various types of stress, which the reason why some individuals take supplements

containing selenide. To this date, there is no known role in periodontal disease.

Copper

Copper, or to be precise, cuprous ion, is essential to maintaining iron ions in their biologically useful

form as ferrous ion. It is also an essential component of superoxide dismutase, which is an enzyme that

quickly inactivates superoxide radicals. The dietary reference intake is 900 micrograms each day for

adults.

Copper deficiency is rare, but may cause neutropenia and impaired bone calcification. Given the role of

copper in iron metabolism, it could also result in hypochromic anemia similar to that caused by iron

deficiency.

There are two ways in which copper toxicity can be seen. One form is the acquired form, where intake

of too much copper causes toxicity. Intake of several grams of copper salt will cause fatal hemolytic

anemia, but the more common form is a slow, chronic form of copper poisoning caused by drinking

acidic beverages or milk from copper containers. In this case, gastroenteritis will develop and early onset

liver cirrhosis.

Another possible way of copper toxicity develops as consequence of a genetic defect that causes copper

accumulation in liver and nervous tissue. In Wilson’s disease, this genetic defect causes hepatitis and

gradual deterioration of nerve function. Another sign of this disease might be a yellow discoloring of the

iris-sclera interface called Kayser-Fleischer rings.

Interestingly, Freeland and others (1976) found that out of all micronutrients, copper was the only

micronutrient with a positive correlation to periodontal disease severity, meaning that patients with

higher serum copper levels also had more periodontal disease.

Manganese

Manganese ions are needed at 2.3 milligrams per day, and they are important cofactors for a variety of

enzymes. They also play a role in bone structure development. There is no known deficiency, and

toxicity is usually associated with jobs involving manganese handling, where it can cause neurologic

symptoms similar to Wilson or Parkinson disease.

There is no known effect on periodontal disease.

Molybdenum

Regarding deficiency, toxicity and periodontal effects, Molybdenum ions are similar to Manganese. The

dietary reference intake value is 45 micrograms per day, and is an important enzyme cofactor for

enzymes metabolizing xanthine, sulfites and aldehydes.

Chromium

Although chromium ions can be extremely toxic, the body needs a miniscule amount of chromium for

normal sugar and fat metabolism, and chromium deficiency can lead to a diabetes-like state. Clinically

more important, many medications can result in chromium insufficiency, and chromium supplements

can enhance effect of beta-blockers, corticosteroids, insulin, nicotinic acid and NSAIDs. The dietary

reference intake is 35 micrograms per day, and chromium is enriched in foods like yeast, liver, cheese

and whole grains.

There is no known effect on periodontal disease.

Co-enzyme Q10

Co-enzyme Q10 is a popular supplement, but there is no recommended value as most human tissues

synthesize sufficient amounts of it for normal life and meats and vegetable oils contain co-enzyme Q10.

In a cohort of subjects in Denmark, the average daily intake was about 3 to 5 milligrams per day.

Co-enzyme Q10 is an important redox partner in mitochondria, and as a good redox partner, it is also a

good antioxidant. It also plays a role in acidification lysosomes, allowing breakdown of ingested material

by cells.

There is no known deficiency or toxicity, but coenzyme Q10 supplementation can decrease the

effectiveness of Warfarin or Coumadin.

There is no known effect on periodontal disease. Given its potential as antioxidant, different researchers

tried applying it topically to gingival tissues during non-surgical therapy to see if it reduces inflammation.

Unfortunately, there are no conclusive results as there either was no effect at all, or only a slight

decrease in inflammation (Hanioka T et al 1994; Hans M et al. 2012)

Lipoic Acid & L-Carnitine

Another set of popular antioxidants are lipoic acid and L-carnitine. As with coenzyme Q10, the human

body synthesizes these in sufficient amounts, and there is no known deficiency syndrome for either one.

A recent animal study showed that a combination of lipoic acid and vitamin C seemed to reduce bone

resorption somewhat in an experimental rat periodontitis model.

For L-carnitine, there is no known role in periodontal disease.

Micronutrients and Periodontics

So, in general the evidence for using dietary supplements to help with periodontal disease treatment is

rather poor (Figure 10). The best evidence we have seen is for Vitamin B complex, Vitamin D, Calcium

Zinc and Omega-3 fatty acids supplements, where small to moderate improvements in healing were

observed in a randomized clinical trial after flap surgery. However, the studies vary widely in quality, and

overall results needs to be used with caution.

Despite the historical association of Vitamin C and scurvy, we did not find any strong evidence for a role

of Vitamin C in treatment of common periodontal diseases.

LEVEL OF EVIDENCE: MICRONUTRIENT &

PERIDONTITIS PREVENTION/TREATMENT B-CSystematic

reviewRandomized

Clinical Trial

Cohort studies

Case-Control studies

Cross-sectional studies

Case reports & series

Animal studies & Benchtop experiments

Rat studies: Omega-3 FA, Vitamin C, D, E, Calcium

Omega-3/PUFA Vitamin D, Calcium

Vitamin C

Vitamin B1,B3, B5, B6

combination

Magnesium, Copper

Zinc

LEVEL OF EVIDENCE: MICRONUTRIENT &

PERIDONTITIS PREVENTION/TREATMENT B-C

Rat studies: Omega-3 FA, Vitamin C, D, E, Calcium

Figure 10. Evidence grade for the use of micronutrients to prevent periodontal disease or

enhance periodontal treatment

Dietary Counseling for Oral Health

Now that we have reviewed necessary nutrients, how does this

translate into a healthy diet that supports systemic and oral

health?

Risky Eating and Identifying Patients at Risk for

Malnutrition We know that nutritional deficiencies and excesses can lead to

frank disease, and that even subtle nutritional insufficiencies

may result in suboptimal tissue functions such as impaired

immunity. If tissues are not functioning properly, you will have

signs and symptoms of disease, and that has been recognized

widely by many cultures and across the ages, even though it

may have lacked scientific rationale.

As there are many ways of achieving minimal nutritional

requirements while satisfying individual and cultural tastes,

there are many ways and ideas of healthy eating.

Recommendations of dietary intake values in this presentation

stem from the U.S. Department of Agriculture’s best scientific

attempt of coming up with nutrition amounts, which also has

been popularized by different food pyramids published over the last decades.

People also look for nutritional guidance to communities that have historically achieved longevity with

low rates of chronic diseases. Examples of these would be the Mediterranean diet with a focus on

unsaturated fatty oils, citrus, vegetables and lean protein sources such as fish and aged cheeses.

Another example is the diet practiced by Okinawans, again with a focus on vegetables and fish as a lean

source of protein.

Partly of ethical, but also physical and spiritual health reasons, vegetarian diets derived from European

and Indian cuisines have attracted a large following, again with a focus on vegetables and non-meat

based sources of protein.

Beyond these there are countless other diets and fads that people follow, in search of good nutritional

advice.

Now, the goal of a dentist is not write new nutrition guide books, or to prescribe a certain diet. You are

not being trained to be registered, licensed dietitians. However, your have three roles when it comes to

nutrition. First, your task is to spot dental patients who also might have nutritional deficiencies, and

refer them to a physician for further evaluation and referral to a dietitian. This is similar to instances

where you identify undiagnosed medical conditions and refer patients for further medical evaluation.

LEARNING

OBJECTIVES - RECALL CHARACTERISTICS

OF A HEALTHY DIET - IDENTIFY ROADBLOCKS

THAT PREVENT HEALTHY

EATING GIVEN A CASE - IDENTIFY PATIENTS AT RISK

FOR MALNUTRITION GIVEN

A CASE - IDENTIFY SIGNS OF

MALNUTRITION - DIFFERENTIATE BETWEEN

FOOD DIARIES AND

QUESTIONAIRES - RECOGNIZE WHEN TO REFER

TO A PHYSICIAN / DIETITIAN

GIVEN A CASE ADVISE A

PATIENT ON NUTRITION FOR

ORAL HEALTH

The second role you have as a dentist is to identify patients where their oral condition is caused or

worsened by nutritional habits, and counsel them on nutrition in order to treat their oral condition. This

is similar to a patient who smokes and who complaints about discolored teeth, where you might provide

tobacco cessation counseling. Lastly, as a health care professional you should promote a healthy lifestyle

that reduces the risk of disease. For that reason you should exemplify and advise patient on healthy

living, and that includes maintaining a healthy diet.

So, what constitutes a healthy diet? In general, healthy diets feature the following characteristics: First,

caloric intake is appropriate for the individual activity level. So you would not recommend a diet

restricted to 500 calories to a construction worker lifting heavy loads all day.

Second, healthy diets tend to include a variety of foods. The all-you-can-eat bacon diet probably is not

that good for you, and probably as bad the all you have is broccoli diet.

Third, healthy diets tend to contain a large proportion of plant-derived foods, which supply most

essential fatty acids, vitamins, caloric value and volume.

Fourth, healthy diets often contain a small amount of lean meat, eggs or fish for a good supply of

essential amino acids and certain vitamins. It is possible to eliminate meat from a diet if one wishes to

do so, but you most likely will have to supplement your diet with various types of dairy, or intelligent

combinations of various beans, grains and vitamin supplements.

Lastly, healthy diets contain little added sugars, salt, alcohol, trans-fats and saturated fats.

As you can see, a healthy diet is not so much about eliminating foods from your diet, but changing the

proportions of your diet.

But why is eating right hard to do?

Typical road blocks to a healthy diet include the following:

Not enough time – the best, healthiest meal is the one you cook fresh for yourself as you are in charge

of the ingredients, and since it is freshly made, it is more likely to contain sensitive nutrients. But making

your own meals can take time, and not everyone can cook. Therefore, the temptation is eating out or

going through the drive-thru, where meals are often pre-cooked, and where meals are loaded with salt

and fat to entice your ancient hunger for calories.

Expense – making your own food may be more expensive as it involves utensils and buying groceries.

Also, high quality foods such as lean meat, certain dairy products and fresh fruit can be pricey depending

where you live. However, in the long run it is cheaper as you eliminate the cost of someone preparing

your food, and unprocessed foods cost less per pound.

Lack of access – in many neighbor hoods there may not be a grocer who has fresh vegetables or meats.

Habit/culture can also work against you. If your culture developed a cuisine that was meant to ensure

survival of individuals working hard out in the fields, but your lifestyle now is that of an office drone

working your finger muscles as main activity, your diet will turn you into a 500 lb bag of lard in no time.

Poverty can prevent you from eating healthy in more than one way. Of course, if you have no money

you cannot buy the food you want. You tend to live in a poorer area where groceries are scarce, and

there won’t be a farmers market selling the freshest organic carrot. You may not have a car, or a car that

only sporadically runs, and you cannot get to a place that sells food. You may not have a kitchen or

utensils to make food since you cannot afford a place that has these things. You may be sicker than

other people which limits your energy to seek out food and prepare it. In any way, being poor sucks in

more way than one, and eating right is not your greatest worry, but survival is.

Not knowing much will also hold you back, as it may feed into poverty, and it may prevent you from

realizing that living of TV dinners may not be that good for you.

Lastly, recreational drugs may suppress your urge to feed yourself, but may also trigger eating binges, or

supply your body with empty calories through alcohol. Either way, you are not going to get the foods

you need.

You can distill these roadblocks into warning signs that a patient in a dental office may be at risk for

malnutrition. From the medical history, the following might warrant further consideration:

= Significant chronic medical conditions putting the patient in a American Society of Anesthesiology Risk

Category greater than two: The reason for this if you have a severe chronic medical condition, you may

be too tired to seek out and prepare your own food.

= Recent unexplained weight gain/loss. This indicates an imbalance of caloric intake versus metabolic

need. It simply may indicate a change in lifestyle, and nutrition has not kept up with, or it might also

indicate onset of an undiagnosed medical condition such as diabetes , or even cancer.

= Pregnant adolescents: Pregnant women experience an increased need of nutrients to support the

developing fetus, but adolescents may suppress their hunger in order to hide a potentially unwanted

pregnancy.

= Disability. As explained before, disability may limit your ability to seek out food due to lack of money,

transportation or energy.

= Alcohol and drug abuse as mentioned before.

= History of increased frequency of colds/infections. Often the immune system is weakened through

nutritional deficiencies, causing more frequent infections.

You may also see the following signs and symptoms that may suggest nutritional deficiency during the

evaluation of a patient:

If a patient complains that their dental condition prevents them from eating, malnutrition is likely.

Unusually severe periodontal disease may also be linked to nutritional deficiency, especially if the

disease is in proportionate to plaque levels, lacks obvious systemic and local etiologic factors, and does

not favor any particular area.

Lingual tooth erosions that cannot be explained other than being caused by eating disorders may also

suggest a higher risk of malnutrition.

Unkempt appearance may indicate an inability to care for oneself, including an inability to feed oneself.

Poverty in the form that a patient has no money for simple, inexpensive dental procedures may also

indicate money for food is tight.

Transportation issues for dental appointments may also indicate a lack of transportation to food

sources.

And lastly, nutrition should be

considered in cases of

unexpectedly poor healing.

There are a couple formal

screening tools one can use.

Posner BM and others (Figure

11, 1993) published this

screening tool that is intended

for older adults who live

independently. Depending on

how many “yes” answers you

get, the higher the risk.

Figure 11. Posner’s Nutrition Screening Initiative Checklist

For patients in nursing homes or those who are incapacitated, Rubenstein Z et al. 2001and others also

published this assessment that relies more on signs than symptoms of nutrition (Figure 12). A low score

here points to malnutrition.

On the other side of the spectrum, malnutrition is a concern in adolescents. For this purpose, another

tool checks for risky nutritional habits (California Department of Public Health Nutritional Risk Screening

Tool, 2000; see Figure 13).

Figure 12. Mini-nutritional assessment short form (MNA-SF, by Rubenstein Z et al. 2001)

If the screening score is less than 12 points, malnutrition should be considered.

Figure 13. The CA DoPH Nutritional Risk Screening Tool (2000)

Analyzing a Patient’s Diet & Suggesting Changes So you identified a patient at risk for malnutrition. How do you find out what their nutritional challenge

is?

If you suspect an eating disorder based on dental findings or using one of the screening tools, don’t

waste time and refer to a medical provider for further referral. Taking care of these things is outside of

your scope of practice, and insurance will not cover a dietitian unless prescribed by a physician.

If you identify a “moderate risk” patient using the screening tools, you should educate the patient about

nutrition, oral health and overall health, and consider investigating the issue further with diaries or

questionnaires, and see if you can suggest changes in their diet. Depending on severity, you still may

want to refer the patient to a physician if there are any systemic signs of malnutrition

If the patient is low risk, encourage maintaining current habits and provide information to the patient as

you see fit and your patient requests it.

There are two ways of checking a patient’s diet. One is by the use of diary where the patient keeps a

detailed record of all foods, snacks and drinks, recording time and amounts. For homemade or specialty

foods, patients may have to count ingredients. If it is processed food or fast food by a major chain,

recording the brand and name of the meal can allow you looking up nutrition information.

Have the patient do this for 3 to 7 days, and you have a highly diagnostic tool that may also educate the

patient on nutritional changes he or she has.

Unlike the prospective diary, questionnaires are retrospective, and can be be obtained preprinted from

places like the California Department of Public Health, where the patient just checks of what they eat.

This is easily interpreted using the USDA food pyramid, but the patient may not remember everything

they ate.

Once you obtain this data, you now analyze it and recommend changes if needed

If the patient has a high snacking frequency, you either get a high caries risk with starchy, sticky, sugary

foods and an added obesity risk if foods are fatty, starchy or sugary.

If the patient drinks a lot of acidic beverages like soda, there is a caries and tooth erosion risk

Excess meat, fat, sweets, cereal intake may lead to obesity risk and the associated risks of obesity such

as type 2 diabetes mellitus, cardiovascular disease and periodontal disease.

Vitamin deficiencies are likely if the fruit/vegetable count is low, and poor wound healing and

exaggerated periodontal disease may happen during therapy.

Low dairy count may increase osteoporosis risk unless there is calcium supplementation or other foods

containing calcium such as tofu. With osteoporosis, there is also an increased risk of periodontal

attachment loss.

Low meat/poultry/fish count may indicate a risk for protein and iron deficiency, which could lead to

poor wound healing.

Once you identify risk areas, you best present this in a motivational interview technique (Figure 14,

Miller and Rollnick 2012). Essentially in this process, you go through four stages: Engaging, Focusing,

Evoking and Planning. Engaging a patient is critical as in this step you establish trust and a working

relationship with a patient as further counseling steps will not be successful without it. Often than not,

the engaging step will already have occurred prior to nutritional counseling during the initial dental visit.

The next step, focusing, may also have been accomplished already in some patients, as now the

question becomes what goals the patient has, and if your goals differ from that of the patient. The

important aspect is that it should feel at this point that you and your patient can work together to

achieve your patient’s goals such as “better teeth”, “healthier gums”, “better healing” or “better

appearance”. In a third step, you should find out what motivates the patient to change, and if there is

any intrinsic factor that a patient possesses which could drive change. In this evoking step, you need to

be careful not to lecture a patient about diet, or to pull a patient into accepting any diet changes.

Change has to come from the patient and not from you. In the last step, you want to facilitate a

patient’s own plan for nutritional change by offering needed information and support. In this planning

stage, you have to be careful not to prescribe changes, and you should step back to allow a patient to

come up with his or her own solutions. This is important as diet changes are much more likely to happen

if there is an intrinsic motivator. In contrast, you trying to badger patients into accepting nutrition

changes likely will cause a reaction, and you are more likely to lose this patient as the door for change

slams shut.

Figure 14. Analysis and Motivational Interviewing

1. Identify malnourished patients and refer to physician for physical

evaluation and referral to dietitian

2. Gather Information on Food Intake and Activity Level for about 5 days

a. Diary (Prospective)

b. Questionnaire (Retrospective)

3. Review Food Intake

a. Meets minimum levels of macro & micronutrients?

b. Adequate calorie intake; Appropriate for activity level?

c. Diabetes/Cardiovascular disease risk

d. Caries risk

4. Motivational Interviewing:

a. Engaging

b. Focusing

c. Evoking

d. Planning

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